1 Facial Palsy BANDAR AL-QAHTANI, M.D. KSMC

2 Etiology Past theories: vascular vs. viral McCormick (1972) – herpes simplex virus Murakami (1996) 11/14 patients with HSV-1 in neural fluid None in controls or Ramsay-Hunt syndrome Temporal bone section at autopsy Animal model inoculated with HSV-1

3 Evaluation Careful history – timing HX of present illness Associated symptoms (pain, dysgeusia) SNHL, vesicles, severe pain Trauma, acute or chronic OM, recurrent Exposures Physical exam Audiometry CT/MRI/other Topographic Electrophysiology

4 Anatomy Intracranial Meatal Labyrinthine (2-4 mm) Tympanic (11 mm) Mastoid (13 mm) Extracranial

5 Anatomy

6 Traumatic facial nerve palsy/paralysis Birth trauma Penetrating injury Iatrogenic Temporal bone # Longitudinal vs transverse or mixed Transection vs edema injury Immediate or delayed

7 Infection Herpes virus,TB..etc Otitis media,cholesteatoma,mastoiditis

8 Metabolic & systemic DM Guillian barre syndrome Autimmune

9 Bell’s Palsy Facial paralysis Acute onset, limited duration, minimal symptoms, spontaneous recovery Idiopathic in past Diagnosis of exclusion Most common diagnosis of acute facial paralysis

10 Pathophysiology HSV viral reactivation leading to damage of facial nerve Neuropraxia– no axonal discontinuity Axonotmesis Wallerian degeneration (distal to lesion) Axoplasmic disruption, endoneural sheaths intact Neurotmesis Wallerian degeneration (distal to lesion) Axon disrupted, loss of tubules, support cells destroyed

11 Electrophysiology Treatment plan based on 16% of patients who do not fully recover Several tests used for prognosis Measure amounts of neural degeneration occurred distal to injury by measuring muscle response to electrical stimulus NET, MST, ENoG, EMG Able to differentiate nerve fibers undergoing Wallerian degeneration

12 Electrophysiology NET (nerve excitability test) Compares current thresholds to elicit minimal muscle contraction 3.5 mA difference significant MST (maximum stimulation test) Compares responses generated with maximal electrical stimulation judged as difference in facial movement

13 Electrophysiology ENoG (electroneuronography) Most accurate, objective Records summation potential Degree of degeneration is directly proportional to amplitudes of measured potentials Done after Wallerian degeneration starts (3-4 days) Compare each day

14 Electrophysiology ENoG Esslen (1977) – over 90% degeneration on ENoG prognosis worsens 90-97%: 30% recover fully 98-99%: 14% recovery fully 100%: none recovered fully Fisch (1981) 50% with % degeneration by 14 days have poor recovery High likelihood of further degeneration if reaches 90% Thus, if ENoG reaches 90% within 2 weeks: recovery

15 Electrophysiology EMG (electromyography) Not useful in acute phase except as complementary test Will be flat with neuropraxia, 100% degeneration, and early regeneration Key in long-term evaluation (over 3 weeks) Fibrillation potentials– degeneration Polyphasic motor units– regenerating nerve

16 Medical Management Eye protection Steroids

17 Medical Management Antivirals Adour (1996)– double blind Only 20% progressed to complete paralysis Acyclovir had less degrees of facial weakness Acyclovir had lower incidence of House 3-5

18 Surgical Management debate over years No surgery Immediate decompression when complete

19 Surgical Management Fisch and Esslen (1972)– 12 patients Total facial nerve decompression via middle cranial fossa and transmastoid Found conduction block at meatal foramen (94% patients) Fisch (1981) Decompression within 14 days for 90% degeneration for maximum benefit May (1979) Transmastoid decompression beneficial (decreased SF, Schirmer’s, MST reduced) May (1984) No patients benefited from surgery within 14 days

20 Surgical Management Gantz (1999)– multi-institutional review Assess if patients with degeneration over 90% within 14 days would benefit Middle cranial fossa (meatal foramen to tympanic segment) If conductive block not identified (6%)– transmastoid added 92% with surgery recovered to House % without surgery to House 1-2

21 ANY QUESTIONS